Transcript Neurocritical care - Greater Sydney Area HEMS

Neurocritical care for
retrieval medicine
Stuart Lane
Overview
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Traumatic Brain Injury
Subarachnoid haemorrhage
Arteriovenous Malformation
Intracranial Haemorrhage
Ischaemic stroke
Specific therapies
Monitoring and drains
Extras
TBI
SAH
AVM
ICH
e.g. vasospasm
TBI
• The leading cause of death and morbidity from ages 1- 44yrs old
• The latest Brain Trauma Foundation (BTF) guidelines 2007 are
well accepted
• Prehospital
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Hypoxaemia and hypotension
GCS used in pre-hospital setting DISCUSS GCS
Non-use paralysis for intubation
Hypertonic NaCl for GCS <8 can be considered
Hyperventilation for signs of herniation
• Penetrating injury also included
• Initial medical management no different
• Surgical management different
• Most likely to be blunt closed TBI
Interhospital transfer
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Avoid hypotension and hypoxaemia
Hypotension is worse than hypoxaemia
Dramatically worsen outcome
Intubation is assumed for this presentation
Oxygen PaO2 > 90mmHg / SpO2 > 95%
PaCO2 35-40 mmHg / PETCO2 31-35 mmHg
CPP cant be assessed without an ICP monitor
MAP > 8O mmHg if no monitor
CPP 50-70 if monitor.
What do we mean by CPP?
What did the trials really show / ?ARDS
Interhospital transfer
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Phenytoin only if witnessed seizure
Resuscitation to euvolaemia with isotonic crystalloids, then use
noradrenaline to augment MAP FLUIDS
NGT / OGT
Normothermic
If spine cleared, then sit 30° head up
Brown tape vs.. white tape
Remove collar and use sandbags – venous congestion
Avoid hyperglycaemia – not really a retrieval issue
Paralyse for transfer
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No evidence of improving ICP
Significant amount of movement for retrieval
BTF not in retrieval patients
Paralysis not evidenced, not worried about CIPMN at this time
May make the patient more CVS stable
ICP monitoring and EVD’s
ICP monitoring and EVD’s
ICP monitoring and EVD’s
• The transducer is fixed at a reference level
• Foramen magnum / external auditory meatus.
• The system is connected to a drainage
chamber
• Allows drainage of CSF into the collecting bag or
chamber.
• The height of this drainage chamber can be
adjusted relative to the reference point
• When the EVD is unclamped and the stopcock is opened it
allows drainage of CSF
• When the ICP is more than the set height of the draining
chamber.
• The drainage will continue until
• The ICP falls to a value less than the chamber height
• The EVD is clamped.
ICP monitoring and EVD’s
• P1- Percussion wave
– Created by systolic blood
pulsation transmitted
through choroid plexus)
• P2- Tidal wave
– Reflects brain compliance
– Exceeds P1 in
noncompliant brain
• P3- Dicrotic wave
– Produced due to aortic
valve closure
ICP monitoring and EVD’s
• A waves - plateau waves
– Lasting 5–20 min
– 50 –100 mmHg high
• B wave
– Frequency of 0.5–2 min-1
– Up to 50mmHg
• C waves
– Last 4–5 min-1
– Up to 20mmHg
• Intervention is required for
A and B waves
• C waves may be
– Normal
– Due to a change in the
vasomotor tone.
Closed vs open EVD
• Limit clamping of EVD’s
• Administration of intrathecal antibiotics
• Assessment for removal
• Getting the patient into a chair / back into bed
• Clamp it whilst transferring the patient from
bed to stretcher
• Avoid loss of csf if the drain goes below the level of
required drainage
• Open it again and leave open for transfer
• For a long transfer, if known ICP problems, then measure
ICP and check pupils at intervals
• Clamp it again when transferring the patient from
stretcher to bed
What if the ICP goes up
• Recheck everything
• ABC and glucose
• Monitoring equipment including waveform
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Deepen sedation
Paralyse, if not already done
Deepen sedation further
Consider CSF drainage / open drainage system
Osmotherapy
• Mannitol vs. hypertonic saline
• Manual hyperventilation in an emergency
Second line ICP therapy
• ABC again
• Recheck the waveform if you have one
• If ICP remains > 20 mmHg for 15 minutes
despite the above treatment
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More sedation
Optimise fluids.
Consider diuresis
EVD left open
Mild hypothermia
More paralysis
Thiopentone bolus
Maintain MAP with noradrenaline
Forget about..
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Transcranial Doppler
Jugular bulb monitoring
Brain oxygen content monitor
Cerebral microdialysis
Corticosteroids
SAH
• 5% of all strokes
• 10–15% die before reaching hospital
• Pathophysiology
– 80% aneurysmal,
– 15% AVM
– 5% other e.g. clotting abnormalities / drugs
• Rebleeding risk
– 8% in the first 48 hours
– 1% per day thereafter
• Reasonable to delay surgery
– Poor grade
– Established vasospasm
Grading systems
Aneurysmal SAH
• Management different if aneurysm is secured or
unsecured
• Much extrapolation of TBI data
• Oxygen PaO2 > 90mmHg / SpO2 > 95%
• PaCO2 35-40 mmHg / PETCO2 31-35 mmHg
• Fluid resuscitation to euvolaemia with isotonic
crystalloid
• Noradrenaline to maintain MAP >70mmHg
• EVD for hydrocephalus ?CLOT DISRUPTION
• Debatable for prevention of hydrocephalus
• ICP monitoring for severe cases
• OGT / NGT
Surgery
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Surgery within 48hrs if possible
Clipping vs.. coiling still a big debate
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Clipping still favoured in the US
Discussion between neurosurgeon and neuroradiologist
Can still Transfer to any neurosurgical centre
Coiling favoured
– Improved mortality with coiling
– Rebleeding slightly higher in coiling group
– Patients with poor clinical grade
– Patients who are medically unstable
– In situations where aneurysm location imparts an increased surgical risk
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• cavernous sinus
• basilar tip aneurysms
Small-neck aneurysms in the posterior fossa
Patients with early vasospasm
Cases where the aneurysm lacks a defined surgical neck
Patients with multiple aneurysms in different arterial territories if surgical
risk is high
• It is falling out of favour once again in some groups
Transfer of aneurysmal SAH
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MAP 70 if aneurysm not secured
30° head up
Keep normothermic
Avoid hyperglycaemia
Nimodipine can wait TRIALS
Magnesium can wait TRIALS
Monitoring and access
CVC and arterial lines discussed later
Vasospasm
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Delayed narrowing of the large capacitance vessels at the base of the
brain
Poorly understood (DOES IT EXIST)
Normally 7-10 days post SAH
70% of SAH patients have angiographic evidence
30% have significant clinical sequelae
Impaired autoregulation
– Cerebral ischaemia
– Cerebral infarction
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Prevention and treatment are different entities
Prevention
– Nimodipine
– Magnesium
– No other agents
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HHH therapy is therapy not treatment
– Illogical
– Not supported
Vasospasm
• Treatment
• Fluids to euvolaemia
• Try to avoid excess hypervolaemia
• Imaging to rule out other possible problems
• Titrate MAP to neurological improvement with
noradrenaline
• MAP 90-100 if unconscious
• Angiography
• Verapamil / papaverine injections
• Angioplasty
AVM
• The direct connection between the
arterial and venous systems supplies a
low-resistance shunt for arterial blood
and exposes the venous system to
abnormally high pressures
• Use systolic BP limitations
• Lots of sedation and paralysis for
transfer
ICH
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10% of all strokes
Surgical intervention becoming less common
Posterior fossa lesions > 3cm
Young patients with lobar haemorrhage
Association with a structural vascular lesion
STITCH trial
• Craniotomy for superficial clots (<10mm from
the skull) with clinical deterioration
• Aspiration for deep clots
rFVIIa for ICH CHANGE CLIPS
rFVIIa for ICH
rFVIIa for ICH
Transfer of ICH
• Specific guidelines
• MAP <130mmHg in chronic hypertension
• No use of rVIIa
• Extrapolation of TBI data once again
• Sedate
• Paralyse
Ischaemic stroke
• 85% of all strokes
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Thrombosis
Embolism
Hypoperfusion
Venous occlusion
• Clinical presentation
• Decreased conscious level
• CT showing
• No haemorrhage
• No significant MCA territory involvement
Thrombolysis?
• Severe neurological
impairment with
NIH stroke scale
>22
• CT evidence of
extensive MCA
territory infarct
• Sulcal effacement
• Loss of GW
differentiation
• Greater than 1/3 MCA
territory
NIH stroke scale
• Total score out of 44
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Level of consciousness
Best gaze
Visual
Facial palsy
Motor arm
Motor leg
Limb ataxia
Sensory
Language
Dysarthria
Extinction and inattention
• If retrieval required
• Likely to be greater than 22
• Unable to assess accurately
Thrombolysis
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Within the first 3 hours
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Within 3-4.5 hours
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MRI of the extent of the infarct core
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Intra-arterial fibrinolytic therapy in 3 to 6 hours
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Based on NINDS 1 and NIND 2 rt-PA trials
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substantial net benefits for virtually all patients with
potentially disabling deficits.
moderate net benefits when applied to all patients with
potentially disabling deficits.
can likely increase the therapeutic yield of lytic therapy,
especially in the 3 to 9 hour window.
moderate net benefits when applied to all patients with
potentially disabling deficits and large artery cerebral
thrombotic occlusions.
For transfer
• Have the primary hospital discuss this
with the receiving hospital
• IV rt-PA
• Aspirin if no haemorrhage on CT
• Anticoagulation not indicated unless
suggestion of venous infarction
– Dose of clexane for transfer
• Specialist interventional radiology
centre for intra-arterial thrombolysis
– New techniques
Other possibilities..
• Hemicraniectomy for significant MCA
infarct
• Treat as for raised ICP
• Surgery is definitive treatment
• 18-60 years within 48 hours
• More likely to be called when
thrombolysis has caused haemorrhagic
transformation
• Cryoprecipitate infusion
• Platelet transfusion
• Primary centre to arrange pre-arrival
Other conditions
• Cerebral tumours
• Consider steroids for raised ICP
• Mannitol is effective
• Cerebral abscess
• Consider steroids for raised ICP
Monitoring
• Arterial line
• Desirable
• Not if delaying treatment
• Central Venous Catheter
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Desirable
For multiple infusions (Not in retrieval medicine)
For catacholamines
CVP measurement is wasting time and useless
Not if delaying treatment
• Don’t delay treatment
• Heavy sedation, may require catacholamines
• Paralysis may help here
Clinical monitoring of possible
cerebral herniation
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Difficult if sedated / paralysed
Pupils need to be seen
So do not tape
Clinical examination remains paramount
Emergency measures
• Hyperventilation
• Osmotherapy
• Burr hole
Clinical monitoring of possible
cerebral herniation
• Can occur at ICP’s <25mmHg
• ICP threshold is not uniform
• Depends on the location of the mass
lesion
• Abnormal posturing on presentation
• Pupillary abnormalities
Brain herniation syndromes
• Supratentorial
herniation
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1 Uncal
2 Central (transtentorial)
3 Cingulate (subfalcine)
4 Transcalvarial
• Infratentorial
herniation
– 1Upward (upward
cerebellar)
– 2 Tonsillar (downward
cerebellar)
Summary
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Keep it simple for transfer
Maintain brain perfusion
Use MAP’s appropriate to pathology
Most specific therapies can wait
Monitoring remains clinical, with
assistance from numbers
• Avoid delays with primary patholgies
Questions?
Questions?